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1.
Biomed Instrum Technol ; 57(2): 67-74, 2023.
Article in English | MEDLINE | ID: mdl-37343111

ABSTRACT

Background: Telemetry monitoring is intended to improve patient safety and reduce harm. However, excessive monitor alarms may have the undesired effect of staff ignoring, silencing, or delaying a response due to alarm fatigue. Outlier patients, or those patients who are responsible for generating the most monitor alarms, contribute to excessive monitor alarms. Methods: Daily alarm data reports at a large academic medical center indicated that one or two patient outliers generated the most alarms daily. A technological intervention aimed at reminding registered nurses (RNs) to adjust alarm thresholds for patients who triggered excessive alarms was implemented. The notification was sent to the assigned RN's mobile phone when a patient exceeded the unit's seven-day average of alarms per day by greater than 400%. Results: A reduction in average alarm duration was observed across the four acute care telemetry units (P < 0.001), with an overall decrease of 8.07 seconds in the postintervention versus preintervention period. However, alarm frequency increased significantly (χ23 = 34.83, P < 0.001). Conclusion: Implementing a technological intervention to notify RNs to adjust alarm parameters may reduce alarm duration. Reducing alarm duration may improve RN telemetry management, alarm fatigue, and awareness. More research is needed to support this conclusion, as well as to determine the cause of the observed increase in alarm frequency.


Subject(s)
Clinical Alarms , Humans , Monitoring, Physiologic , Telemetry , Intensive Care Units , Patient Safety
2.
J Nurs Adm ; 53(3): 175-180, 2023 Mar 01.
Article in English | MEDLINE | ID: mdl-36753439

ABSTRACT

OBJECTIVES: The aim of this study was to increase patient safety during care transitions through the development of a new process and electronic screening tool. BACKGROUND: Direct hospital admissions that are not clinically triaged can put the patient at an increased safety risk. METHODS: Utilizing the electronic medical record and mnemonic situation, background, assessment, and recommendation (SBAR), an admission module was created to intake direct admission requests by transfer center nurses to ensure clinical triage and accurate bed placement. RESULTS: One hundred eighty-nine direct admissions met inclusion criteria. Thirteen patients were clinically screened, deemed not stable for the acute care setting, and sent to the emergency department. One direct admission safety event occurred involving a hypoglycemic patient upon arrival. Results indicate the new clinical screening program offered a safer way to directly admit patients to the inpatient setting. CONCLUSION: Implementation of the electronic SBAR handoff tool meets the Joint Commission standard of care transitions compliance. The significant workflow changes increased patient safety and will be expanded in the future to all service lines.


Subject(s)
Hospitalization , Patient Handoff , Humans , Emergency Service, Hospital , Triage , Critical Care , Inpatients , Patient Admission
3.
Cell Rep Med ; 3(10): 100783, 2022 10 18.
Article in English | MEDLINE | ID: mdl-36260981

ABSTRACT

Harnessing innate immunity is emerging as a promising therapeutic approach in cancer. We report here the design of tetraspecific molecules engaging natural killer (NK) cell-activating receptors NKp46 and CD16a, the ß-chain of the interleukin-2 receptor (IL-2R), and a tumor-associated antigen (TAA). In vitro, these tetraspecific antibody-based natural killer cell engager therapeutics (ANKETs) induce a preferential activation and proliferation of NK cells, and the binding to the targeted TAA triggers NK cell cytotoxicity and cytokine and chemokine production. In vivo, tetraspecific ANKETs induce NK cell proliferation and their accumulation at the tumor bed, as well as the control of local and disseminated tumors. Treatment of non-human primates with CD20-directed tetraspecific ANKET leads to CD20+ circulating B cell depletion, with minimal systemic cytokine release and no sign of toxicity. Tetraspecific ANKETs, thus, constitute a technological platform for harnessing NK cells as next-generation cancer immunotherapies.


Subject(s)
Interleukin-2 , Neoplasms , Animals , Interleukin-2/genetics , Killer Cells, Natural , Receptors, Interleukin-2/metabolism , Cytokines , Neoplasms/genetics , Chemokines/metabolism
4.
Cell ; 175(7): 1731-1743.e13, 2018 12 13.
Article in English | MEDLINE | ID: mdl-30503213

ABSTRACT

Checkpoint inhibitors have revolutionized cancer treatment. However, only a minority of patients respond to these immunotherapies. Here, we report that blocking the inhibitory NKG2A receptor enhances tumor immunity by promoting both natural killer (NK) and CD8+ T cell effector functions in mice and humans. Monalizumab, a humanized anti-NKG2A antibody, enhanced NK cell activity against various tumor cells and rescued CD8+ T cell function in combination with PD-x axis blockade. Monalizumab also stimulated NK cell activity against antibody-coated target cells. Interim results of a phase II trial of monalizumab plus cetuximab in previously treated squamous cell carcinoma of the head and neck showed a 31% objective response rate. Most common adverse events were fatigue (17%), pyrexia (13%), and headache (10%). NKG2A targeting with monalizumab is thus a novel checkpoint inhibitory mechanism promoting anti-tumor immunity by enhancing the activity of both T and NK cells, which may complement first-generation immunotherapies against cancer.


Subject(s)
Antineoplastic Agents, Immunological/therapeutic use , Carcinoma, Squamous Cell , Cetuximab/therapeutic use , Immunity, Cellular/drug effects , Immunotherapy , Killer Cells, Natural/immunology , NK Cell Lectin-Like Receptor Subfamily C , Animals , CD8-Positive T-Lymphocytes/immunology , CD8-Positive T-Lymphocytes/pathology , Carcinoma, Squamous Cell/immunology , Carcinoma, Squamous Cell/pathology , Carcinoma, Squamous Cell/therapy , Clinical Trials, Phase II as Topic , Humans , Killer Cells, Natural/pathology , Mice , NK Cell Lectin-Like Receptor Subfamily C/antagonists & inhibitors , NK Cell Lectin-Like Receptor Subfamily C/immunology
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